ArticlePsychopharmacology2004
In vitro inhibition of recombinant ligand-gated ion channels by high concentrations of milnacipran.
Article in Psychopharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Allosteric modulators of the α4β2 subtype of neuronal nicotinic acetylcholine receptors.Biochemical pharmacology · 2011Review
- Modulation of ligand-gated ion channels by antidepressants and antipsychotics.Molecular neurobiology · 2007Review
- Stimulation of catecholamine synthesis via activation of p44/42 MAPK in cultured bovine adrenal medullary cells by milnacipran.Naunyn-Schmiedeberg's archives of pharmacology · 2007Article
- Japanese experience with milnacipran, the first serotonin and norepinephrine reuptake inhibitor in Japan.Neuropsychiatric disease and treatment · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleTricyclic antidepressants are known to inhibit various ligand-gated ion-channel (LGIC) receptors, and some of their clinical features may be associated with this activity. The effects of milnacipran, a selective inhibitor of the reuptake of serotonin and noradrenaline, on LGIC receptors have not yet been investigated on such ion-channel receptors.
objectivesTo determine the in vitro effect of milnacipran on four recombinant LGIC receptors, nicotinic acetylcholine, N-methyl-D-aspartate, gamma-amino butyric acid (GABA) and 5-hydroxytryptamine3A receptors.
methodsReceptors were expressed in Xenopus oocytes and LGIC activity measured using a two-voltage clamp technique.
resultsThere was no interaction at the GABA receptor. The results at the other LGIC receptors showed that they could be inhibited by high concentrations of milnacipran.
conclusionsAt high concentrations, milnacipran can inhibit certain LGICs. It is, however, unlikely that these interactions have any clinical consequence under normal therapeutic conditions, since the concentrations required are considerably higher than those achieved in plasma of treated patients.
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